Evidence against role of antidiuretic hormone in support of blood pressure during dehydration.

Abstract

The contribution of arginine vasopressin (AVP) to the maintenance of mean arterial pressure (MAP) during fluid deprivation was reinvestigated in chronically prepared, conscious, freely moving rats. In normal Long-Evans (LE) rats during water deprivation for up to 48 h plasma AVP levels increased from 2.98 +/- 0.62 to 17.55 +/- 2.03 pg/ml, but MAP and heart rate (HR) remained unchanged. Fluid deprivation for 10 h in Brattleboro homozygous rats that are unable to synthetize vasopressin resulted in a more severe water depletion than 48 h of dehydration in the normal rats, but also in this group MAP and HR were maintained at values not significantly different from control. Cardiac output (CO) fell during the course of dehydration in both LE and Brattleboro rats. Injection of 20 micrograms/kg of the vasopressin pressor antagonist, 1-deamino-penicillamine, 2-(O-methyl)-tyrosine AVP [dPTyr(Me)AVP] did not decrease MAP or increase HR in LE rats after 24 h of water deprivation and was ineffective even after 48 h of fluid deprivation. CO also remained unchanged following AVP blockade. Efficacy of the antagonist was verified by complete inhibition of the pressor response elicited by exogenous AVP. The concentration of plasma catecholamines was unaltered by dPTyr(Me)AVP. Blockade of the renin-angiotensin system via converting-enzyme inhibition failed to reveal any depressor effect after injection of dPTyr(Me)AVP. Thus it appears that AVP is not involved in the maintenance of blood pressure after fluid deprivation in conscious rats.